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Novel synthetic analogue of ACTH 4-10 (Semax) but not glycine prevents the enhanced nitric oxide generation in cerebral cortex of rats with incomplete global ischemia.

Abstract
This work investigates whether nitric oxide production and lipid peroxidation contribute to the pathophysiology of ischemia and whether glycine and a novel Russian compound, Semax are neuroprotective via a mechanism involving the regulation nitric oxide (NO) and lipid peroxidation. In brief, nitric oxide and indices of lipid peroxidation were elevated following global ischemia. While glycine proved ineffective in reducing NO levels or ameliorating the neurological deficits following global ischemia, Semax proved to be highly effective in abating the rise in nitric oxide and restoring neurologic functioning.
AuthorsV G Bashkatova, V B Koshelev, O E Fadyukova, A A Alexeev, A F Vanin, K S Rayevsky, I P Ashmarin, D M Armstrong
JournalBrain research (Brain Res) Vol. 894 Issue 1 Pg. 145-9 (Mar 09 2001) ISSN: 0006-8993 [Print] Netherlands
PMID11245825 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
Chemical References
  • Nootropic Agents
  • Peptide Fragments
  • Nitric Oxide
  • ACTH (4-7), Pro-Gly-Pro-
  • Adrenocorticotropic Hormone
  • ACTH (4-10)
  • Glycine
Topics
  • Adrenocorticotropic Hormone (analogs & derivatives, chemistry, pharmacology)
  • Animals
  • Brain Ischemia (metabolism)
  • Cerebral Cortex (drug effects, metabolism)
  • Glycine (pharmacology)
  • Lipid Peroxidation (drug effects, physiology)
  • Male
  • Nitric Oxide (metabolism)
  • Nootropic Agents (pharmacology)
  • Peptide Fragments (chemistry, pharmacology)
  • Rats
  • Rats, Wistar

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